Protective effect of dexamethasone on fetal rat skin in experimental intrauterine ischaemia/reperfusion injury.

BACKGROUND: Perinatal asphyxia is an important cause of injury to fetal tissues such as the brain, heart, liver and gastrointestinal system. Fetal skin has also been shown to be vulnerable to intrauterine injury after intrauterine ischaemia/reperfusion (I/R) injury. AIM: To examine the effect of dexamethasone on fetal skin in intrauterine I/R injury in rats. METHODS: The response of rat fetal skin to I/R injury and maternal dexamethasone treatment were assessed by determining thiobarbituric acid reactive substances (TBARS), and myeloperoxidase (MPO) and nitric oxide (NO) metabolites. We also examined the ultrastructural changes of fetal skin. Bilateral utero-ovarian artery clamping was performed to produce ischaemia for 30 min in rats at day 19 of pregnancy, and reperfusion was achieved by removing the clamps for 60 min before fetal tissue was collected. The treatment group was given dexamethasone intraperitoneally 20 min before I/R was performed. RESULTS: TBARS, MPO and NO all increased significantly in fetal rat skin after I/R injury. Levels of TBARS, MPO and NO were significantly lower in the dexamethasone-treated group than in the I/R-only group. I/R injury produced ultrastructural damage in the epidermis. Oedema and mitochondrial damage were less severe in the dexamethasone-treated group. CONCLUSIONS: Maternal treatment with dexamethasone may have a protective effect on fetal skin in cases of I/R injury.

Effect of intrauterine ischaemia-reperfusion injury on rat skin.

INTRODUCTION: It was previously demonstrated that decreased maternal blood flow might create impairment in skin development. The aim of this study was to show by means of lipid peroxidation the effect of intrauterine ischaemia-reperfusion injury on fetal rat skin. METHODS: In total, 24 female Spraque-Dawley rats, 19 days pregnant, were used. They were separated into three groups (n = 8): a control group, a sham-operated group and an experimental group. Laparotomy was performed on all three groups. In the sham-operated and experimental groups, utero-ovarian artery dissection was performed in addition. In the experimental group, fetal ischaemia was induced by clamping the utero-ovarian artery bilaterally for 30 min, and reperfusion was achieved by removing the clamps for 60 min. At the end of the experiment, the fetuses were removed by caesarean section and skin specimens were taken from the fetuses. Lipid peroxidation in the skin tissues was determined as thiobarbituric acid reactive substance (TBARS) concentration for each fetal rat. One-way ANOVA and post hoc tests were used for statistical analysis. RESULTS: The level of TBARS was significantly increased in the fetal rat skin after ischaemia-reperfusion injury compared with the control group. CONCLUSION: Lipid peroxidation has an important role in intrauterine ischaemia-reperfusion-induced fetal skin damage in rats.

Possible impact of inflammatory status on C-telopeptide pyridinoline cross-links of type I collagen and osteocalcin levels around oral implants with peri-implantitis: a controlled clinical trial.

Detection of progression level of peri-implantitis may help in the prevention of oral implant failure. C-telopeptide pyridinoline crosslinks of Type I collagen (ICTP) and osteocalcin (OC) are specific markers of bone turnover and bone degradation. Determination of the ICTP and OC levels in the peri-implant sulcus fluid (PISF) may predict the metabolic and/or inflammatory changes in the peri-implant bone. The aim of this clinical study was to evaluate ICTP and OC levels in the PISF for oral implants with and without peri-implant bone destruction and correlate these levels with the traditional clinical peri-implant parameters (probing depth, plaque index, gingival index and gingival bleeding time index) and radiographic bone level measurements. Fifteen patients with 30 peri-implant sites with bone destruction (radiographic bone loss) and health were included. Clinical parameters were measured and PISF was collected from the sites. Peri-implant sulcus fluid ICTP and OC levels were detected by radioimmunoassay technique from PISF samples. All clinical parameters demonstrated a significant increase in peri-implantitis sites compared with healthy sites. The PISF volume of the peri-implantitis sites was also significantly higher than of the healthy peri-implant sites. Although not statistically significant, a trend of increase was demonstrated in ICTP PISF samples sampled from peri-implantitis sites compared with healthy sites. A significant increase was noticed for OC PISF level in peri-implantitis sites compared with healthy ones. As well as peri-implant clinical measurements, volumetric changes at PISF may be counted as an important clinical parameter to distinguish the bone destruction sites from healthy sites around oral implants.

Cobaltous ion inhibition of lipid peroxidation in biological membranes.

The effect of cobalt on lipid peroxidation in biological membranes, phospholipid liposomes and fatty acid micelles was investigated. Cobaltous ion, at micromolar concentrations, inhibited iron-ascorbate induced lipid peroxidation in erythrocyte ghosts, microsomes and phosphatidylserine liposomes at pH 7.4. The pH seemed to be important for the anti-peroxidative effect of cobalt, because under slightly acidic conditions cobalt did not inhibit peroxidation. Cobalt was less effective in inhibiting peroxidation stimulated by organic hydroperoxides. Iron-ascorbate induced lipid peroxidation was also inhibited by EDTA. However, certain ratios of EDTA: cobalt in the reaction mixture stimulated peroxidation. Cobalt did not inhibit lipid peroxidation in linoleic acid micelles and phosphatidylethanolamine liposomes. The presence of phosphatidylserine, however, rendered these micelles and liposomes to cobalt inhibition. We conclude that the cobaltous ion is a potent inhibitor of lipid peroxidation in biological membranes and that the binding of cobalt to phosphatidylserine is necessary for the inhibitory effect of this metal ion.

Angiotensin converting enzyme gene polymorphism and activity in Turkish patients with essential hypertension.

Studies in various ethnic groups have shown contradictory evidence on the association of the angiotensin converting enzyme (ACE) insertion/ deletion (I/D) polymorphism with essential hypertension. We conducted a case-control study in Samsun, Turkey, to examine the association between ACE genotype, ACE serum activity, and blood pressure. Serum ACE activity was measured and ACE I/D polymorphism performed in 165 hypertensive and 143 normotensive subjects. Genomic DNA was extracted from blood samples and amplified by polymerase chain reaction (PCR). PCR primers were flanking the polymorphic region in intron 16 of the ACE gene. The distribution of the DD, ID, and II ACE genotypes was 65, 77, and 23 in hypertensive patients and 42, 82, and 19 in normotensive subjects (P > .05). The estimated frequency of the insertion allele was 0.37 in hypertensive and 0.42 in normotensive subjects. Nevertheless, sensitivity analysis, based on positive family history and severity of hypertension, suggested that significant associations existed between more homogeneous groups of hypertensives and normotensives (P < .05). ACE genotype influenced ACE activity and the highest level was in DD genotype, being the lowest in II genotype. ACE serum levels were significantly higher in hypertensives as compared with normotensives (P < .01). A modest correlation was observed between blood pressure and ACE among hypertensive persons (r = 0.25, P < .05) and this did persist in multivariate analysis (P < .05 for systolic blood pressure and P < .005 for diastolic blood pressure). These data suggest that ACE DD genotype may have predisposing effects on severe hypertensives and cases with positive family history, and that ACE may be one of the independent factors on hypertension.

Ipsilateral and contralateral testicular biochemical acute changes after unilateral testicular torsion and detorsion.

OBJECTIVES: An experimental study has been conducted to investigate testicular blood flow alterations through acute biochemical changes during unilateral testicular torsion and detorsion. METHODS: One hundred twenty male albino rats were divided into 12 groups, each containing 10 rats. One group served to determine basal values of biochemical parameters, 4 groups were subjected to varying periods of unilateral testicular torsion (3, 6, 12, and 24 hours, respectively), 3 groups were subjected to detorsion following varying periods of torsion (6, 12, and 24 hours, respectively), and 4 groups underwent sham operations as controls. Levels of lactic acid, hypoxanthine, and lipid peroxidation products were determined in testicular tissues. RESULTS: Values of these 3 parameters obtained from sham operation control groups did not differ significantly from basal values (p > 0.05). All 3 parameters were increased significantly in both ipsilateral torted and contralateral nontorted testes after unilateral testicular torsion when compared with basal values (p < 0.05). Detorsion did not cause significant changes in levels of lipid peroxidation products in both ipsilateral torted and contralateral nontorted testes when compared with values obtained after torsion (p > 0.05). CONCLUSIONS: Ipsilateral testicular torsion causes a decrease not only in the ipsilateral torted but also in the contralateral nontorted testicular perfusion. The clues of reperfusion injury do not become evident following detorsion of testicular torsion lasting more than 6 hours.

Time-level relationship for lipid peroxidation and the protective effect of alpha-tocopherol in experimental mild and severe brain injury.

OBJECTIVE: Oxygen free radical-mediated lipid peroxidation has been proposed to be one of the major mechanisms of secondary damage in traumatic brain injury. The first purpose of this study was to establish the time-level relationship for lipid peroxidation in injured brain tissue. The second purpose was to examine the protective effect of alpha-tocopherol against lipid peroxidation. METHODS: For this study, 65 guinea pigs in five groups were studied. Five of the animals were identified as a control group, and the remaining 60 animals were divided equally into four groups (Groups A, B, C, and D). Mild injury (200 g x cm) (Groups A and C) and severe injury (1000 g x cm) (Groups B and D) were produced by the method of Feeney et al. Alpha-tocopherol (100 mg/kg) was administered intraperitoneally before brain injury in Groups C and D. Five animals from each group were killed immediately after trauma, five after 1 hour, and the remaining five animals after 36 hours. Lipid peroxidation in traumatized brain tissues was assessed using the thiobarbituric acid method. RESULTS: In all groups with traumatic brain injuries, levels of malondialdehyde, a lipid peroxidation product, were higher than in the control group. The amount of lipid peroxidation was increased by the severity of the trauma. Alpha-tocopherol significantly suppressed the rise in lipid peroxide levels in traumatized brain tissues. CONCLUSION: This study demonstrates that lipid peroxidation is increased by the severity of trauma and that alpha-tocopherol has a protective effect against oxygen free radical-mediated lipid peroxidation in mild and severe brain injury.

Effect of melatonin on cerebral edema in rats.

OBJECTIVE: Melatonin (5-methoxy-N-acetyltrypamine), a chemical naturally produced in the pineal gland, has been suggested to be a free radical scavenger and an antioxidant. In the present study, the effect of melatonin on cold-induced brain edema was evaluated by determination of cerebral water content, blood-brain barrier permeability, and areas of infarct; the effects were also studied histopathologically. METHODS: Brain edema was produced in rats by creating a lesion via cortical freezing. Animals were separated into four groups: sham-operated (craniectomy only); control (cold injury); sham-vehicle (cold injury plus saline); and melatonin treatment (cold injury plus melatonin). Melatonin was administered (50 mg/kg intraperitoneally) 15 minutes after the cold injury was induced. Twenty-four hours later, tissue samples from the core, from the periphery of the cold-injured hemisphere, and from the contralateral hemisphere symmetrical to the cold injury were obtained. RESULTS: Melatonin treatment reduced edema (mean +/- standard deviation; 86.22 +/- 1.54% in the control group versus 80.78 +/- 2.76% in the melatonin treatment group, P < 0.001) and blood-brain barrier permeability (45.34 +/- 2.75% in the control group versus 38.26 +/- 3.40% in the melatonin treatment group, P < 0.001) at the periphery of cold injury. Area of infarct reduced from 5.84 +/- 0.58% in the control group to 3.30 +/- 0.89% in the melatonin treatment group (P < 0.001). The effect of melatonin was also confirmed histopathologically. CONCLUSION: Melatonin was found to be neuroprotective in instances of cold-induced brain edema. Thus, melatonin may be a valuable therapeutic agent in the treatment of cerebral edema.

Comparison of the effects of melatonin and methylprednisolone in experimental spinal cord injury.

OBJECT: Melatonin is a very effective antioxidant agent. This study was performed to investigate the effects of melatonin in experimental spinal cord injury (SCI). The authors also compared its effects with those of methylprednisolone, which also protects the spinal cord from secondary injury because of its antioxidant effect on membrane lipids. METHODS: Adult male albino rats were used for the study, and paraplegia was produced using a previously described weight-drop technique. Melatonin and methylprednisolone were given intraperitoneally by bolus injections of 100 mg/kg and 30 mg/kg, respectively, immediately after induction of trauma. The animals were killed, and 1-cm samples of injured spinal cord were obtained at 1, 24, and 48 hours postinjury. Lipid peroxidation was estimated by thiobarbituric acid test. Electron microscopic studies were performed to determine the effects of melatonin on neurons, axons, and subcellular organelles after experimental SCI. A grading system was used for quantitative evaluation. Following SCI, there was significant increase in lipid peroxidation. In melatonin- and methylprednisolone-treated groups, lipid peroxidation was found to decrease to the baseline (preinjury) levels. There was a significant difference between trauma-alone and treatment groups, but no statistical difference was found between the melatonin- and methylprednisolone-treated groups. Electron microscopic findings showed that SCI produced by the weight-drop technique resulted in profound tissue damage. CONCLUSIONS: Both melatonin and methylprednisolone have been shown to protect neuron, axon, myelin, and intracellular organelles including mitochondrion and nucleus. However, this study provides quantitative evidence that this protection of neurons and subcellular organelles of spinal cord after secondary injury is much more obvious in melatonin-treated rats than those treated with methylprednisolone. In view of these data, melatonin has been shown to be very effective in protecting the injured spinal cord from secondary injury.

The importance of data presentation regarding gingival crevicular fluid myeloperoxidase and elastase-like activity in periodontal disease and health status.

BACKGROUND: The enzymatic profile of gingival crevicular fluid (GCF) is being analyzed with increasing interest, but related studies lack a general consensus on most methodological points, including the appropriate mode of data presentation. METHODS: GCF myeloperoxidase (MPO) and elastase-like activity (ELA) levels were spectrophotometrically determined on a total of 60 subjects who were divided into three equal subgroups as early-onset periodontitis (EOP), adult periodontitis (AP), and healthy. GCF enzyme levels were calculated and evaluated both as total enzyme activity and enzyme concentration. The correlations between these GCF enzymes and clinical periodontal status were also analyzed. RESULTS: With both modes of data presentation, the results regarding MPO activity were consistent. When presented either as total MPO activity or MPO concentration, the periodontally healthy group showed significantly lower MPO activity than the two patient groups (P<0.05). However, two modes of data presentation did not match when GCF ELA was concerned. When data were reported as total ELA, the healthy group exhibited lower enzyme activity (0.02 +/- 0.001 U) than EOP (0.04 +/- 0.01 U) and AP (0.06 +/- 0.02 U) groups; but when reported as concentration, the highest ELA levels were seen in the healthy group (221 +/- 31.53 nmol/min/ml), followed by AP (98.63 +/- 23.03 nmol/min/ml) and EOP (70.49 +/- 12.02 nmol/min/ml) (P<0.05). A strong-positive and significant correlation existed between GCF MPO and ELA. Correlations with clinical parameters were mostly observed with total activities. CONCLUSIONS: The findings of the present study confirm the relationship between GCF ELA and MPO activity and periodontal disease and also support the functional relativity between the two enzymes. Furthermore, based on these findings, it can be suggested that data presentation by use of total activity seems to be more sensitive in both the reflection of the actual enzymatic profile of GCF and also the existing clinical periodontal status. For each GCF component, the validity of different modes of data presentation should be considered.

Analysis of human gingival tissue and gingival crevicular fluid beta-glucuronidase activity in specific periodontal diseases.

BACKGROUND: Beta-glucuronidase (betaG) is one of the enzymes involved in the destruction of non-collagenous components of the extracellular matrix. It is also considered an indicator or predictor of periodontal disease activity. The present study was conducted to determine the presence and the levels of betaG activity in gingival tissue and gingival crevicular fluid (GCF) in periodontal disease and health status. The validity of 2 expressions of data, total betaG activity versus betaG concentration, and the correlations between clinical periodontal status and betaG profile was also evaluated. METHODS: betaG activities in gingival tissues and GCF samples from 57 individuals, divided into 3 equal groups of adult periodontitis (AP), early-onset periodontitis (EOP), and periodontally healthy subjects were spectrophotometrically examined. RESULTS: Both patient groups had higher betaG levels in both gingiva and GCF than controls. Significant differences were observed among all groups when total GCF betaG activities were examined (P <0.05). However, the difference between AP and controls was not significant when concentration values were compared (P >0.05). The highest GCF betaG activity, with both expressions, was detected in EOP group. No absolute correlations between clinical parameters and betaG activity were observed, except for random correlations in the patient groups with mean total betaG activities. Also GCF/gingiva betaG levels and the 2 expressions did not show absolute correlations. CONCLUSIONS: The findings of the present study confirm the relationship between betaG activity and periodontal diseases. The differences in data concerning GCF total betaG activity and betaG concentration may suggest that they are not matching measures. Data presentation seems to be an important factor in GCF/enzyme profile studies.

A study of adenosine treatment in experimental acute spinal cord injury. Effect on arachidonic acid metabolites.

STUDY DESIGN: A prospective, randomized, blinded experimental trauma study. STUDY OBJECTIVE: The effect of adenosine on arachidonic acid metabolites and lipid peroxidation was investigated in induced spinal cord injury. SUMMARY OF BACKGROUND DATA: Effects of adenosine in ischemia-reperfusion models have been studied, but no studies of adenosine's effect on direct trauma to the spinal cord have been reported. METHODS: Thirty-seven adult Wistar albino rats were randomly divided into four groups and underwent laminectomy. Group 1 underwent a sham operation. Group 2 received an intravenous adenosine infusion of 100 micrograms/kg per minute for 30 minutes. In Group 3, a standard spinal cord trauma of 50 g.cm strength was established at the lower thoracic level with a "weight-drop" technique, and Group 4 received an infusion of adenosine (100 micrograms/kg per minute) for 30 minutes after the trauma. RESULTS: Tissue prostaglandin E2 activity was significantly higher in adenosine-treated trauma groups when compared with that in other groups (P < 0.0001). The difference in tissue leukotriene C4 activity between control and trauma groups was significant (P < 0.05). Adenosine infusion after trauma limited the increases in lipid peroxidation, with the difference approaching significance at P = 0.06. The structure of myelin was well preserved in the adenosine-treated trauma group. However, the changes were irreversible in severely damaged areas. CONCLUSION: After acute spinal cord trauma, intravenous adenosine infusion of 100 micrograms/kg per minute could attenuate progression to secondary injury, but adenosine alone was not effective yet.

Ultrastructural effect of sildenafil citrate on corpus cavernosum and other genital organs in female rats.

AIM: To determine the ultrastructural effects of sildenafil on the female genital organs. METHODS: Twenty female cycling Wistar albino rats weighing 250+/-20 g were randomly divided into two groups of 10 each. Rats of one group were gavaged with 0.5 mg.kg(-1).d(-1) of sildenafil 3 days in a week for 4 weeks and the other served as the controls. After cessation of treatment animals were sacrificed by cervical dislocation under methoxyflurane anaesthesia. The clitoris, vagina, uterus and bartholin glands were taken at the estrous and were fixed with 10% formalin solution for light microscopy and 2.5% glutaraldehyde and osmic acid for electron microscopy. RESULTS: Under the light microscope, the fibrocollageous tissue was found increased, the capillaries enlarged and the connecting tissue elements increased in the corpus cavernosum in the treated group. On electron microscopy, increased connective tissue, fibroblasts with notched nucleus, shorten immature collagen fibers without striation were seen. Abundant foldings and penetration with collagen bundles were observed in the basal membrane. Large connection complexes, especially gap junctions among the wide capillary endothelial cells were observed. CONCLUSION: There are evident histological changes due to sildenafil citrate in female rat corpus cavernosum. The clitoris and bartholin glands were the most effected organs. While the histopathological changes of clitoral tissue could be expected, an increase in the mass of bartholin gland was surprising.

Detection of head and neck cancer with 99Tc(m) glutathione: a correlative study with tissue glutathione and glutathione S-transferase levels.

In this study glutathione (GSH), a natural tripeptide which plays an important role in detoxification reactions, protecting cells against damage from xenobiotics, has been labelled with 99Tc(m) for the demonstration of head and neck cancer. Twenty-eight patients (10 females and 18 males) with various malignancies of the head and neck were given 740 MBq of 99Tc(m)-GSH intravenously and single-photon emission computed tomography (SPECT) images were obtained at 3 h. Semiquantification was performed by drawing regions of interest on three consecutive transaxial slices and tumour to background ratios were calculated. In addition, GSH and glutathione S-transferase (GST) levels were measured in the tumour samples and in normal tissue which were obtained during surgery. Scintigraphic images showed that there was increased uptake in the tumour compared to the normal contralateral side (tumour/normal tissue (mean +/- SD) = 1.94 +/- 0.76). The tissue analyses revealed increased levels of GST in tumour tissues, but both GST and GSH levels in tumour were not statistically different from those in the normal tissue. We conclude that scintigraphic visualization of head and neck tumours can be attributed to increased demand for GSH in cancer. Protein binding might account for the prolonged retention of 99Tc(m)-GSH in the malignant tissue. Like other peptides, it is accumulated and excreted by the kidneys, which allows clear visualization of the abdomen without interference from gastrointestinal system activity.

C-Reactive protein as a risk factor for left ventricular thrombus in patients with acute myocardial infarction.

BACKGROUND: Elevated C-reactive protein (CRP) has been found to correlate with higher risk for cardiac events in patients with acute myocardial infarction (AMI). It has been suggested that CRP may be involved in initiation process of coagulation; however, the role of CRP level in the formation of left ventricular (LV) thrombus has not been studied. HYPOTHESIS: This study investigated whether CRP is a risk factor for LV thrombus in patients with AMI. METHODS: Clinical, echocardiographic, and biochemical data were analyzed in 141 consecutive patients (aged 57 +/- 13 years; 33 women) with first anterior AMI. Two-dimensional and Doppler echocardiographic examinations were performed on Days 1, 3, 7, 15, and 30. Blood samples were obtained every day during hospitalization. Serum CRP concentrations were measured by an ultrasensitive immunonephelometry method. RESULTS: Left ventricular thrombus was detected in 33 (23.4%) patients. Univariate analysis showed that patients with LV thrombus had a higher peak creatine kinase (CK) level (2,879 +/- 742 vs. 1,693 +/- 1,210 I/U, p = 0.001), higher peak CRP level (14.9 +/- 7.1 vs. 9.2 +/- 6.8 mg/dl, p = 0.001), higher wall motion score index (1.8 +/- 0.2 vs. 1.5 +/- 0.3, p = 0.002), higher apical wall motion score index (2.35 +/- 0.72 vs. 2.07 +/- 0.70, p = 0.001), larger end-diastolic volume (145.2 +/- 43.7 vs. 116.5 +/- 44.2 ml, p = 0.002), larger end-systolic volume (85.4 +/- 37.2 vs. 62.9 +/- 31.6 ml, p = 0.003), and lower ejection fraction (42.1 +/- 12 vs. 47.3 +/- 13, p = 0.04). In multivariate analyses, only peak CK level (p = 0.0001), LV apical wall motion score index (p = 0.001), and CRP levels (p = 0.001) were independent predictors of LV thrombus formation. CONCLUSIONS: These results suggest that CRP is a risk factor for LV thrombus in patients with AMI.

Effect of erythropoietin on bcl-2 gene expression in rat cardiac myocytes after traumatic brain injury.

The purpose of this study was to investigate whether erythropoietin (EPO) has an effect on the expression of bcl-2 in rat cardiac myocytes following experimental isolated traumatic brain injury (TBI). Forty-eight Wistar-Albino female rats were randomly allocated into eight groups. Groups AC and BC were controls; groups AS and BS were sham-operated animals. Groups A1 and B1 underwent head trauma without treatment. Groups A2 and B2, head traumas plus EPO intraperitoneally (1000 IU/kg); groups A3 and B3, the vehicle groups, head traumas and intraperitoneal albumin (0.4 ml/rat). The method of weight drop was used to produce impact trauma at 24 hours after injury. Samples obtained from the left ventricle were assayed for lipid peroxidation and bcl-2 gene expression using real-time quantitative polymerase chain reactions. Lipid peroxidation in the heart tissue was determined by the concentration of thiobarbituric acid reactive substances (TBARs). The results showed that administration of EPO significantly reduced the increase in lipid peroxidation by-products after moderate or severe trauma. The bcl-2 expression was significantly higher in EPO (A2 and B2) compared to trauma groups (A1 and B1) suggesting a protective effect. These findings suggest that EPO may play an important role in the expression of bcl-2 and decrease in TBARs-the end product of lipid peroxidation in myocytes-after moderate or severe TBI.

A single dose of erythropoietin attenuates lipid peroxidation in experimental liver ischemia-reperfusion injury in the rat fetus.

OBJECTIVE: The aim of the study was investigate the effectiveness of recombinant human erythropoietin (r-Hu-EPO) in attenuating the severity of experimental liver ischemic injury in fetal rats. METHODS: The animals were divided randomly into four groups. In the control group, fetal whole liver tissue was taken immediately after laparotomy from pregnant animals. In the ischemia-reperfusion (I/R) group, tissue samples were taken immediately after I/R injury. In the vehicle group, 0.4 ml of human serum albumin solution and in the treatment group, r-Hu-EPO (5000 IU/kg) in 0.4 ml of human serum albumin solution were given intraperitoneally, 30 min before I/R injury, as a single dose. Thiobarbituric acid-reactive substances (TBARS) were estimated to demonstrate lipid peroxidation. RESULTS: Lipid peroxidation byproducts increased after I/R injury. Administration of r-Hu-EPO reduced TBARS after I/R injury. CONCLUSION: Further investigations are needed to understand the mechanism of the hepatoprotective effect of erythropoietin and the clinical importance of ischemic liver injury in the fetus.

Protective effect of lisinopril against ischemia-reperfusion injury in isolated guinea pig hearts.

BACKGROUND: In order to determine whether angiotensin-converting enzyme inhibitors (ACEI s) attenuate ischemia-reperfusion injury, we investigated and compared the effects of lisinopril via different routes of administration in an isolated guinea pig heart model of ischaemia reperfusion. METHODS: The effect of lisinopril cardioplegia, oral pretreatment with lisinopril and lisinopril enriched reperfusion solution on myocardium after a normothermic global ischemia of 90 minutes and 30 minutes of reperfusion in the modified Langendorff model was randomly studied in 4 groups (n=8 in each). In all groups, cardioplegic arrest was achieved by administering St. Thomas Hospital Cardioplegic Solution (STHCS). The first group was utilized as the control. In the second group, hearts were arrested with lisinopril (1 micromol/L) enriched STHCS. In the third group, animals were pretreated with oral lisinopril (0.2 mg/kg/twice a day) for ten days. In the last group hearts were again pretreated with oral lisinopril (like in Group 3) and the heart were reperfused with lisinopril enriched (1 micromol/L) Krebs-Henseleit solution during the reperfusion period. RESULTS: Contractility, which was expressed as contractile force (g contractility/g heart weight), was preserved better in the study groups. In the last group, the hearts had the best left ventricular contractile function, where contractile force was 58.4%+/-4.82% of the preischaemic values. In Group I, Group II and Group III they achieved 29.5%+/-5.6%, 41.9%+/-4.9%, and 55.3%+/-5.8% of their preischaemic contractile force values respectively. Creatine kinase leakage was significantly lower and also post- ischaemic coronary flows were significantly higher in the 4th group. Coronary flow after reperfusion increased from 48.0+/-6.2 to 68.0+/-4.51 ml/min.g.heart, in Group IV (p<0.05). CONCLUSIONS: Myocardial MDA and GSH contents showed that there was a correlation between the depletion of myocardial GSH content and increased lipid peroxidation. The myocardial GSH content indicates that the best results were obtained in the last group as compared to the other groups. These preliminary results showed that oral preconditioning improved postischaemic myocardial function and decreased myocardial injury. Because the best results were achieved in the last group, it can be suggested that lisinopril may also play a protective role against reperfusion injury.

The role of lipid peroxidation in the genesis of vasospasm secondary to subarachnoid hemorrhage.

The aim of this study is to find out the possible trigger role of lipid peroxidation in vasospasm. Haemoglobin-free washed erythrocyte membranes (erythrocyte ghost) corresponding to 2.5 mg membrane protein was mixed with 0.5 umol NADPH 3 umol ADP, 4 umol ferrous sulphate and injected into the cisterna magna of cats to stimulate lipid peroxidation in vivo (Group 1). The second group was injected lml/kg whole blood and the control group 1 ml/kg saline. Angiographic studies revealed significant vasospasm in five cats in group 1. Severe vasospasm was seen in six cats in group 2. A significant increase in lipid peroxidation was observed in groups 1 and 2, compared to the control group. These results may suggest that free radical products may play an important role in the complex genesis of vasospasm in subarachnoid haemorrhage.

Tissue hypoxia in ipsilateral and contralateral testes undergoing surgically induced maldescent.

The mechanism of deterioration of ipsilateral and contralateral testes during unilateral maldescent remains controversial. Proposing that alterations in tissue perfusion may play a role in ipsilateral and contralateral testicular deteriorations, an experimental study has been planned to evaluate the status of parameters of tissue hypoxia in ipsilateral and contralateral testes following surgically induced maldescent, in rats which preoperatively underwent placebo or chemical sympathectomy. 60 male albino rats were used for the experiment. At the age of 21 days each 30 rats that were treated by placebo or chemical sympathectomy agent were divided into 3 groups undergoing sham operation, abdominal fixation of one testis or abdominal fixation of both testes. At the age of 3 months the rats underwent bilateral orchidectomies and lactic acid (LA) and hypoxanthine (HX) levels were measured in testicular tissues. Maldescent of the testis resulted in a marked increase of LA and HX values in the ipsilateral testis compared to controls, and also resulted in increased levels of LA and HX in the contralateral testis. Although the levels of LA and HX were lower compared to ipsilateral undescended counterparts the levels in contralateral testis were significantly elevated compared to the contralateral testes of rats undergoing sham operation following placebo treatment. Bilateral maldescent resulted in similar elevations of LA and HX in both of the testes. Administration of 6-hydroxydopamine did not result in decreased levels of LA and HX values in the ipsilateral testis following unilateral testicular undescendence. However the LA levels in the contralateral descended testis did not reveal a significant difference compared to the contralateral testis of rats undergoing sham operation. The present experimental design reveals that abdominal fixation of the testis results in tissue hypoxia not only in the ipsilateral but also in the contralateral testis. Chemical sympathectomy has some protective effects on contralateral testicular hypoxia during unilateral maldescent. Tissue hypoxia during maldescent may result from relative inadequacy of testicular blood flow to overcome the increased metabolic demands under hyperthermic conditions.